Structured Review

Millipore p38 kinases
The effects of PI3K, MEK, JNK and <t>p38</t> inhibitors on TNFα- or HA-mediated β-arrestin 1 and 2 expression in FLS
P38 Kinases, supplied by Millipore, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/p38 kinases/product/Millipore
Average 86 stars, based on 1 article reviews
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p38 kinases - by Bioz Stars, 2021-04
86/100 stars

Images

1) Product Images from "Increased expression of beta-arrestin 1 and 2 in murine models of rheumatoid arthritis; Isoform specific regulation of inflammation"

Article Title: Increased expression of beta-arrestin 1 and 2 in murine models of rheumatoid arthritis; Isoform specific regulation of inflammation

Journal: Molecular immunology

doi: 10.1016/j.molimm.2011.07.021

The effects of PI3K, MEK, JNK and p38 inhibitors on TNFα- or HA-mediated β-arrestin 1 and 2 expression in FLS
Figure Legend Snippet: The effects of PI3K, MEK, JNK and p38 inhibitors on TNFα- or HA-mediated β-arrestin 1 and 2 expression in FLS

Techniques Used: Expressing

2) Product Images from "Purinergic inhibition of Na+,K+,Cl− cotransport in C11-MDCK cells: Role of stress-activated protein kinases"

Article Title: Purinergic inhibition of Na+,K+,Cl− cotransport in C11-MDCK cells: Role of stress-activated protein kinases

Journal: Purinergic Signalling

doi: 10.1007/s11302-007-9057-z

Effect of ATP and anisomycin on JNK and p38 phosphorylation ( a ) and NKCC ( b ) in C11 cells. 100 μM ATP and 0.1 μM anisomycin were added during the last 40 min of preincubation of cells in Cl − -depleted medium. Phosphoprotein content and NKCC activity in the absence of ATP and anisomycin were taken as 1.0 and 100%, respectively. Mean values from three ( a ) or four ( b ) independent experiments are shown
Figure Legend Snippet: Effect of ATP and anisomycin on JNK and p38 phosphorylation ( a ) and NKCC ( b ) in C11 cells. 100 μM ATP and 0.1 μM anisomycin were added during the last 40 min of preincubation of cells in Cl − -depleted medium. Phosphoprotein content and NKCC activity in the absence of ATP and anisomycin were taken as 1.0 and 100%, respectively. Mean values from three ( a ) or four ( b ) independent experiments are shown

Techniques Used: Activity Assay

Representative blots revealing the effects of SP600125 ( a ), MPA ( b ), SB202190 ( c ), and SB202474 ( d ) on JNK and p38 phosphorylation in C11 cells under control conditions and in the presence of 100 μM ATP or 0.1 μM anisomycin. ATP and anisomycin were added during the last 40 min of preincubation of cells in Cl − -depleted medium. Compounds SP600125, MPA, SB202190, and SB202474 were added at the indicated concentrations 30 min before ATP or anisomycin
Figure Legend Snippet: Representative blots revealing the effects of SP600125 ( a ), MPA ( b ), SB202190 ( c ), and SB202474 ( d ) on JNK and p38 phosphorylation in C11 cells under control conditions and in the presence of 100 μM ATP or 0.1 μM anisomycin. ATP and anisomycin were added during the last 40 min of preincubation of cells in Cl − -depleted medium. Compounds SP600125, MPA, SB202190, and SB202474 were added at the indicated concentrations 30 min before ATP or anisomycin

Techniques Used:

Related Articles

Expressing:

Article Title: Increased expression of beta-arrestin 1 and 2 in murine models of rheumatoid arthritis; Isoform specific regulation of inflammation
Article Snippet: FLS from DBA/1J mice were stimulated with TNFα (10 ng/ml, Sigma), HA (100 µg/ml) and HMGB1 (1 µg/ml, Prospec) for 6 h, 12 h, 24 h and 48 h. After stimulation, the protein was collected to determine β-arrestin 1 and 2 expression in FLS. .. To determine the effects of PI3K, ERK 1/2, JNK and p38 kinases on TNFα- and HA- induced increases of β-arrestin 1 and 2 expression in FLS, cells were pretreated with PI3K inhibitor Wortmannin (10 nM, Calbiochem), MEK inhibitor PD98059 (10 µM, Calbiochem), JNK inhibitor SP600125 (10 µM, Calbiochem) or p38 inhibitor SB203580 (10 µM, Calbiochem) for 1 hour followed by stimulation with TNFα (10 ng/ml) or HA (100 µg/ml) for 24 h. β-arrestin 1 and 2 expression were examined by Western blot analysis. .. The joint tissues were minced and lysed with ice-cold RIPA lysis buffer (10 mM Tris, pH 7.4, 1% Triton X-100, 150 mM NaCl, 1 mM EGTA, 1 mM EDTA, 1 mM phenylmethylsulfonyl fluoride, 1 µg/ml aprotinin, 1 µg/ml leupeptin, and 1 µg/ml pepstatin A).

Article Title: Involvement of FAK/P38 Signaling Pathways in Mediating the Enhanced Osteogenesis Induced by Nano-Graphene Oxide Modification on Titanium Implant Surface
Article Snippet: Molecular Mechanism InvestigationWestern blot analysis was used to detect the molecular mechanisms of the responsive behaviors of BMSCs cultured on the different material surfaces. .. After 48 h of culture, the protein expression of focal adhesion kinase (FAK), phospho-FAK (p-FAK), extracellular signal-related kinase 1/2 (ERK1/2), phospho-ERK1/2 (p-ERK1/2), P38 MAP kinases (P38), phospho-P38 (p-P38), Jun amino-terminal kinase (JNK), and phospho-JNK (p-JNK) were analyzed, and the expression level of β-actin was used as a reference. .. For Western blot analysis, the cells were first lysed by RIPA buffer (Beyotime, China).

Article Title: Novel Therapeutic Targets in Neuroinflammation and Neuropathic Pain
Article Snippet: .. Chaparro-Huerta V, Flores-Soto ME, Gudi-o-Cabrera G, Rivera-Cervantes MC, Bitzer-Quintero OK, Beas-Zárate C. Role of p38 MAPK and pro-inflammatory cytokines expression in glutamate-induced neuronal death of neonatal rats. ..

Western Blot:

Article Title: Increased expression of beta-arrestin 1 and 2 in murine models of rheumatoid arthritis; Isoform specific regulation of inflammation
Article Snippet: FLS from DBA/1J mice were stimulated with TNFα (10 ng/ml, Sigma), HA (100 µg/ml) and HMGB1 (1 µg/ml, Prospec) for 6 h, 12 h, 24 h and 48 h. After stimulation, the protein was collected to determine β-arrestin 1 and 2 expression in FLS. .. To determine the effects of PI3K, ERK 1/2, JNK and p38 kinases on TNFα- and HA- induced increases of β-arrestin 1 and 2 expression in FLS, cells were pretreated with PI3K inhibitor Wortmannin (10 nM, Calbiochem), MEK inhibitor PD98059 (10 µM, Calbiochem), JNK inhibitor SP600125 (10 µM, Calbiochem) or p38 inhibitor SB203580 (10 µM, Calbiochem) for 1 hour followed by stimulation with TNFα (10 ng/ml) or HA (100 µg/ml) for 24 h. β-arrestin 1 and 2 expression were examined by Western blot analysis. .. The joint tissues were minced and lysed with ice-cold RIPA lysis buffer (10 mM Tris, pH 7.4, 1% Triton X-100, 150 mM NaCl, 1 mM EGTA, 1 mM EDTA, 1 mM phenylmethylsulfonyl fluoride, 1 µg/ml aprotinin, 1 µg/ml leupeptin, and 1 µg/ml pepstatin A).

other:

Article Title: Novel Therapeutic Targets in Neuroinflammation and Neuropathic Pain
Article Snippet: The Role of p38 MAPK and Its Substrates in Neuronal Plasticity and Neurodegenerative Disease.

Article Title: Farnesol activates the intrinsic pathway of apoptosis and the ATF4-ATF3-CHOP cascade of ER stress in human T lymphoblastic leukemia Molt4 cells
Article Snippet: The MEK1/ 2 inhibitor U0126 was obtained from Promega (Madison, WI), and the p38 MAPK and JNK inhibitors, SB203580 and SP600125, respectively, were purchased from Calbiochem (La Jolla, CA).

Article Title: Novel Therapeutic Targets in Neuroinflammation and Neuropathic Pain
Article Snippet: Chaparro-Huerta V, Rivera-Cervantes MC, Flores-Soto ME, Gomez-Pinedo U, Beas-Zarate C. Proinflammatory cytokines and apoptosis following glutamate-induced excitotoxicity mediated by p38 MAPK in the hippocampus of neonatal rats.

Transfection:

Article Title: Obesity-associated Inflammation Induces microRNA-155 Expression in Adipocytes and Adipose Tissue: Outcome on Adipocyte Function
Article Snippet: Each transfection reaction contained 240 ng of miR-155 promoter fragment in pGL3-basic vector (Promega) and 5 ng of pGL4.73 (Promega) containing Renilla luciferase for normalization. .. Twenty-four hours after transfection, cells were treated with specific inhibitors of MAP kinases (JNK, p38) and NF-κB signaling (JNK inhibitor II [10μM], SB 202190 [20μM] and BAY 117082 [10μM], respectively) for 1 hour (all obtained from Calbiochem, Merck Millipore) and then stimulated or not with TNFα (15 ng/mL) for 24 hours. .. Both firefly and Renilla luciferase were measured with Dual-Glo Luciferase Assay System (Promega), and firefly activity was normalized with Renilla activity.

Purification:

Article Title: In Vivo Interaction Proteomics Reveal a Novel p38 Mitogen-Activated Protein Kinase/Rack1 Pathway Regulating Proteostasis in Drosophila Muscle
Article Snippet: FLAG-tagged p38 kinase constructs were transfected into S2 cells, and cells were stimulated with 10 mM H2 O2 for 45 min. .. Active p38 kinases were purified using anti-FLAG magnetic beads (Sigma) as described previously ( ). .. Kinase reactions were assembled by mixing purified MBP-RACK1 with bead-bound kinases in 25 mM Tris (pH 7.5), 5 mM β-glycerophosphate, 2 mM dithiothreitol (DTT), 0.1 mM Na3 VO4 , 10 mM MgCl2 , and 200 μM ATP.

Magnetic Beads:

Article Title: In Vivo Interaction Proteomics Reveal a Novel p38 Mitogen-Activated Protein Kinase/Rack1 Pathway Regulating Proteostasis in Drosophila Muscle
Article Snippet: FLAG-tagged p38 kinase constructs were transfected into S2 cells, and cells were stimulated with 10 mM H2 O2 for 45 min. .. Active p38 kinases were purified using anti-FLAG magnetic beads (Sigma) as described previously ( ). .. Kinase reactions were assembled by mixing purified MBP-RACK1 with bead-bound kinases in 25 mM Tris (pH 7.5), 5 mM β-glycerophosphate, 2 mM dithiothreitol (DTT), 0.1 mM Na3 VO4 , 10 mM MgCl2 , and 200 μM ATP.

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  • 96
    Millipore p38 mapk inhibitor
    A, Representative CMGs in SCI mice with CSF or <t>p38</t> MAPKi treatment. The number of NVCs was reduced in p38 <t>MAPK</t> inhibitor-treated SCI mice. B, CMG parameters in SCI mice treated intrathecally with CSF or p38 treatment. VE was significantly improved as shown by increases in VV and MP, and a decrease in PVR in p38 MAPK inhibitor-treated SCI mice (P38 treatment) compared with CSF-treated SCI mice. CMG, cystometrogram; CSF, cerebrospinal fluid; MAPK, mitogen-activated protein kinase; MP, micturition pressure; NVC, nonvoiding contraction; p38 MAPKi, p38 MAPK inhibitor; PVR, post-void residual volume; SCI, spinal cord injury; VE, voiding efficiency; VV, voided volume
    P38 Mapk Inhibitor, supplied by Millipore, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/p38 mapk inhibitor/product/Millipore
    Average 96 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    p38 mapk inhibitor - by Bioz Stars, 2021-04
    96/100 stars
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    99
    Millipore sb202190
    The effect of pharmacological inhibition of p38 MAPK on WA-mediated apoptosis in MCF-7 cells. The MCF-7 cells were pretreated with 10 μM <t>SB202190</t> for 1 h, exposed to 2.5 μM WA in the absence or presence of SB202190 for 24 h, and then processed for western blot analysis or apoptosis detection. (A) Western blotting for phosphorylated p38 MAPK and cleaved PARP. Quantitation for phosphorylated p38MAPK relative to DMSO-treated cells is shown. (B) Histone-associated DNA fragment release into the cytosol. Quantitation relative to DMSO-treated cells is shown. Combined results (n = 6) from two independent experiments are shown as mean ± S.D. Statistical significance was determined by one-way ANOVA with Bonferroni’s multiple comparison test. a Significantly different ( P
    Sb202190, supplied by Millipore, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/sb202190/product/Millipore
    Average 99 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    sb202190 - by Bioz Stars, 2021-04
    99/100 stars
      Buy from Supplier

    Image Search Results


    A, Representative CMGs in SCI mice with CSF or p38 MAPKi treatment. The number of NVCs was reduced in p38 MAPK inhibitor-treated SCI mice. B, CMG parameters in SCI mice treated intrathecally with CSF or p38 treatment. VE was significantly improved as shown by increases in VV and MP, and a decrease in PVR in p38 MAPK inhibitor-treated SCI mice (P38 treatment) compared with CSF-treated SCI mice. CMG, cystometrogram; CSF, cerebrospinal fluid; MAPK, mitogen-activated protein kinase; MP, micturition pressure; NVC, nonvoiding contraction; p38 MAPKi, p38 MAPK inhibitor; PVR, post-void residual volume; SCI, spinal cord injury; VE, voiding efficiency; VV, voided volume

    Journal: Neurourology and urodynamics

    Article Title: Role of p38 MAP kinase signaling pathways in storage and voiding dysfunction in mice with spinal cord injury

    doi: 10.1002/nau.24170

    Figure Lengend Snippet: A, Representative CMGs in SCI mice with CSF or p38 MAPKi treatment. The number of NVCs was reduced in p38 MAPK inhibitor-treated SCI mice. B, CMG parameters in SCI mice treated intrathecally with CSF or p38 treatment. VE was significantly improved as shown by increases in VV and MP, and a decrease in PVR in p38 MAPK inhibitor-treated SCI mice (P38 treatment) compared with CSF-treated SCI mice. CMG, cystometrogram; CSF, cerebrospinal fluid; MAPK, mitogen-activated protein kinase; MP, micturition pressure; NVC, nonvoiding contraction; p38 MAPKi, p38 MAPK inhibitor; PVR, post-void residual volume; SCI, spinal cord injury; VE, voiding efficiency; VV, voided volume

    Article Snippet: Also, a limitation of the present study is that a group of SI mice treated with a p38 MAPK inhibitor was not included.

    Techniques: Mouse Assay

    Overview of the potential mechanisms involved in the DpC-mediated effects on neuroblastoma. DpC increases TNFα expression in neuroblastoma cells, which may (1) activate cytotoxic T cells to destroy tumor cells and/or (2) acts on the TNFα receptor ( TNFR ) to activate down-stream signaling pathways. These include the MAPK/p38/JNK and NF-ĸB signaling cascades, which lead to nuclear transcription of numerous genes, including those that induce apoptosis, as well as cytokines such as TNFα. Activation of TNFR also promotes cleavage of caspase 8, leading to caspase 3 cleavage and subsequent apoptosis. Moreover, DpC is also highly redox active, resulting in the production of reactive oxygen species (ROS) [ 13 ]. The generation of ROS triggers the release of cytochrome c from mitochondria [ 8 ], leading to cleavage of caspase 9, which then also cleaves caspase 3, leading to apoptosis. Further, the increased ROS also leads to upregulation of neuroglobin ( Ngb ) and cytoglobin ( Cygb ) expression as both of these proteins respond to oxidative stress. Together, these molecular effects, which promote apoptosis, could contribute to the anti-cancer activity of DpC in neuroblastoma

    Journal: Journal of Hematology & Oncology

    Article Title: The novel thiosemicarbazone, di-2-pyridylketone 4-cyclohexyl-4-methyl-3-thiosemicarbazone (DpC), inhibits neuroblastoma growth in vitro and in vivo via multiple mechanisms

    doi: 10.1186/s13045-016-0330-x

    Figure Lengend Snippet: Overview of the potential mechanisms involved in the DpC-mediated effects on neuroblastoma. DpC increases TNFα expression in neuroblastoma cells, which may (1) activate cytotoxic T cells to destroy tumor cells and/or (2) acts on the TNFα receptor ( TNFR ) to activate down-stream signaling pathways. These include the MAPK/p38/JNK and NF-ĸB signaling cascades, which lead to nuclear transcription of numerous genes, including those that induce apoptosis, as well as cytokines such as TNFα. Activation of TNFR also promotes cleavage of caspase 8, leading to caspase 3 cleavage and subsequent apoptosis. Moreover, DpC is also highly redox active, resulting in the production of reactive oxygen species (ROS) [ 13 ]. The generation of ROS triggers the release of cytochrome c from mitochondria [ 8 ], leading to cleavage of caspase 9, which then also cleaves caspase 3, leading to apoptosis. Further, the increased ROS also leads to upregulation of neuroglobin ( Ngb ) and cytoglobin ( Cygb ) expression as both of these proteins respond to oxidative stress. Together, these molecular effects, which promote apoptosis, could contribute to the anti-cancer activity of DpC in neuroblastoma

    Article Snippet: In studies using cell signaling pathway inhibitors, cells were pre-incubated for 2 h/37 °C with 5 μM of the ERK/MAPK inhibitor, PD98059 (Sigma-Aldrich), 5 μM of the p38 MAPK inhibitor, SB203580 (Sigma-Aldrich), 5 μM of the JNK/MAPK inhibitor, SP600125 (Sigma-Aldrich), 15 μg/mL of the NF-kB inhibitor, CAPE (Sigma-Aldrich), and 10 μM of the pan-caspase inhibitor, Z-VAD(ome)-FMK (Calbiochem, Darmstad, Germany).

    Techniques: Expressing, Activation Assay, Activity Assay

    The effect of pharmacological inhibition of p38 MAPK on WA-mediated apoptosis in MCF-7 cells. The MCF-7 cells were pretreated with 10 μM SB202190 for 1 h, exposed to 2.5 μM WA in the absence or presence of SB202190 for 24 h, and then processed for western blot analysis or apoptosis detection. (A) Western blotting for phosphorylated p38 MAPK and cleaved PARP. Quantitation for phosphorylated p38MAPK relative to DMSO-treated cells is shown. (B) Histone-associated DNA fragment release into the cytosol. Quantitation relative to DMSO-treated cells is shown. Combined results (n = 6) from two independent experiments are shown as mean ± S.D. Statistical significance was determined by one-way ANOVA with Bonferroni’s multiple comparison test. a Significantly different ( P

    Journal: Molecular carcinogenesis

    Article Title: Role of Mitogen-Activated Protein Kinases and Mcl-1 in Apoptosis Induction by Withaferin A in Human Breast Cancer Cells

    doi: 10.1002/mc.22050

    Figure Lengend Snippet: The effect of pharmacological inhibition of p38 MAPK on WA-mediated apoptosis in MCF-7 cells. The MCF-7 cells were pretreated with 10 μM SB202190 for 1 h, exposed to 2.5 μM WA in the absence or presence of SB202190 for 24 h, and then processed for western blot analysis or apoptosis detection. (A) Western blotting for phosphorylated p38 MAPK and cleaved PARP. Quantitation for phosphorylated p38MAPK relative to DMSO-treated cells is shown. (B) Histone-associated DNA fragment release into the cytosol. Quantitation relative to DMSO-treated cells is shown. Combined results (n = 6) from two independent experiments are shown as mean ± S.D. Statistical significance was determined by one-way ANOVA with Bonferroni’s multiple comparison test. a Significantly different ( P

    Article Snippet: Pharmacological inhibitors of MAPK, including SB202190 (p38 MAPK inhibitor), SP600125 (JNK inhibitor), and PD98059 (inhibitor of an upstream kinase in ERK signaling pathway) were purchased from EMD-Millipore (Billerica, MA).

    Techniques: Inhibition, Western Blot, Quantitation Assay

    Synergistic ENaC induction by endiandrin A is linked to an activation of p38 and ERK in HT-29/B6-GR cells. HT-29/B6-GR cells were pre-incubated with the indicated MAPK inhibitors (10 µmol/L) for 1 hour before addition of dexamethasone (1 µM) and/or TNF-α (500 U/ml) and/or endiandrin A (20 µM) for 24 hours. ( A ) Measurement of ENaC-dependent Na + absorption as the drop in I SC after amiloride (100 µM) and measurement of γ-ENaC-mRNA after 24 hours. GAPDH was used for normalization of mRNA expression. Data are given as means ± s.e.m., n = 8–11 and n = 5–8, *** P

    Journal: PLoS ONE

    Article Title: The Plant-Derived Glucocorticoid Receptor Agonist Endiandrin A Acts as Co-Stimulator of Colonic Epithelial Sodium Channels (ENaC) via SGK-1 and MAPKs

    doi: 10.1371/journal.pone.0049426

    Figure Lengend Snippet: Synergistic ENaC induction by endiandrin A is linked to an activation of p38 and ERK in HT-29/B6-GR cells. HT-29/B6-GR cells were pre-incubated with the indicated MAPK inhibitors (10 µmol/L) for 1 hour before addition of dexamethasone (1 µM) and/or TNF-α (500 U/ml) and/or endiandrin A (20 µM) for 24 hours. ( A ) Measurement of ENaC-dependent Na + absorption as the drop in I SC after amiloride (100 µM) and measurement of γ-ENaC-mRNA after 24 hours. GAPDH was used for normalization of mRNA expression. Data are given as means ± s.e.m., n = 8–11 and n = 5–8, *** P

    Article Snippet: Specific inhibitors of MAPK, the p38 MAPK inhibitor SB202190, the p42/44 extracellular signal-regulated kinase (ERK, ERK’s upstream kinase MEK1/2) inhibitor U0126 and the JNK MAPK inhibitor SP600125 (Sigma-Aldrich) were used in a concentration of 10 µM.

    Techniques: Activation Assay, Incubation, Expressing